Early membrane exposure of phosphatidylserine followed by late necrosis in murine macrophages induced by Candida albicans from an HIV-infected individual

Panagio, Luciano Aparecido; Felipe, Ionice; Vidotto, Marilda Carlos; Gaziri, L. C. J.

doi:10.1099/0022-1317-51-11-929

Cited by 13 publications

(19 citation statements)

References 26 publications

(22 reference statements)

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“…Strain 577 was used as a control because our group observed previously that it did not induce apoptosis (Panagio et al , 2002; Gasparoto et al , 2004). Exposure of phosphatidylserine through binding to annexin‐V‐FITC was observed more frequently in macrophage populations from mice pretreated with PBS compared with Con‐A‐activated macrophages after phagocytosis of opsonized C. albicans CR15 (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Recognition by CR3 does not trigger a protective host defence, such as the respiratory burst (Wright & Silverstein 1983; Netea et al , 2008). Considering that C. albicans 577 does not induce macrophage apoptosis (Panagio et al , 2002), it is likely that the three strains tested used the pathway CR3 to establish an appropriate environment for survival within the phagocytic cells.…”

Section: Discussionmentioning

confidence: 99%

“…Candida albicans 577, isolated from the skin of a patient with mucocutaneous candidiasis, was used as a negative control, as it did not induce apoptosis in macrophages. Candida albicans CR1 induced macrophage apoptosis (Panagio et al , 2002) and CR15 was tested in this work.…”

Section: Methodsmentioning

confidence: 99%

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Increased tumour necrosis factor-α production, higher mannose receptor activity and ability to killCandidaby concanavalin-A-activated macrophages

Geraldino

Vito

Custodio

et al. 2010

FEMS Immunol Med Microbiol

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In a previous study, our group verified that mice pretreated with concanavalin-A (Con-A) produced more tumour necrosis factor (TNF)-alpha and presented greater Candida clearance from the peritoneal cavity, liver and spleen, which yielded a higher survival rate than control animals. In this work, the hypothesis that macrophages were of crucial importance in overcoming the infection was tested. Thus, peritoneal macrophages from mice pretreated for 3 days with Con-A or phosphate-buffered saline (PBS) were coincubated with CR1, CR15 and 577 isolates of Candida albicans for 0.5, 1 and 2 h. The ability of Con-activated macrophages to produce TNF-alpha, ingest via mannose receptors and kill all the isolates was significantly greater compared with PBS-treated macrophages, and activated macrophages exhibited a lower incidence of apoptosis, verified by binding to annexin V-fluorescein isothiocyanate. The transition of yeast cells to filamentous forms during coincubation for 2 h with control macrophages was about 73-80%, whereas in the presence of Con-A-activated macrophages, it was 35-40%. Our results suggest that a greater clearance of C. albicans infection through treatment with Con-A is probably due to the activation of macrophages, which produce more TNF-alpha, express more mannose receptors and are better endowed to kill ingested C. albicans.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Increased tumour necrosis factor-α production, higher mannose receptor activity and ability to killCandidaby concanavalin-A-activated macrophages

Geraldino

Vito

Custodio

et al. 2010

FEMS Immunol Med Microbiol

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“…We previously reported that C. albicans CR1, which was isolated from a HIV‐infected individual, induced early apoptotic changes in macrophages that phagocytosed them in vitro, but that those macrophages progressed to necrosis and lysis 2 h thereafter; similar pro‐apoptotic changes were not observed in macrophages co‐incubated with C. albicans 577, which was isolated from skin lesions of an individual not infected with HIV [14]. In this work,we verified that macrophages from the peritoneal exudate of mice that had received an intraperitoneal inoculum of strain CR1 bound annexin V‐FITC and became permeable to propidium iodide, and that these changes occurred from 30 min to 2 h after in vivo infection, in agreement with the prior in vitro observations.…”

Section: Discussionmentioning

confidence: 95%

Apoptosis of phagocytic cells induced byCandida albicansand production of IL-10

Gasparoto

Gaziri

Burger

et al. 2004

FEMS Immunology &Amp; Medical Microbiology

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Macrophages co-incubated with Candida albicans strain CR1 in vitro showed early signs of apoptosis, but evolved to necrosis after 2 h. In this study, we investigated whether strain CR1 caused apoptosis or necrosis of macrophages after its inoculation into mice peritoneal cavity, and whether this correlated with the secretion of IL-10. Peritoneal macrophages from mice that received an inoculum of C. albicans CR1 showed signs of apoptosis and necrosis from 30 min to 2 h afterwards, whereas heat-killed C. albicans did not cause those effects. IL-10 production was low during the first 6 h post-infection, when macrophages predominated in the peritoneal exudate, whereas its higher production after 24 h correlated with an increase of neutrophils in the exudate. Treatment of CR1 with pepstatin (an inhibitor of proteinases) prevented the process of apoptosis and significantly reduced IL-10 production, suggesting that the increased production of IL-10 was caused by processes occurring during the initial phase of infection, such as apoptosis, necrosis and uptake of death cells.

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“…Quality control at the cellular level is known to rely on different signals including the absence of histocompatibility molecules in vertebrates [164] or expression of one of several "eat-me" markers, which -once exposed on the cell exterior -induce phagocytosis, for example through recognition of phosphatidylserine (PS) via CD36-like receptors such as Croquemort (see above and [165]). In addition infected cells may expose PS [166] as do certain viruses, which obtain PS from their host cells in their envelope [167]. In mosquitoes, PS exposure on ookinetes has been observed [168].…”

Section: Endogenous Elicitors Of Immunitymentioning

confidence: 96%

Mechanisms of Drosophila Immunity - An Innate Immune System at Work

Theopold¹,

Dushay

2007

CIR

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Insect immune systems which lack the type of adaptive immunity known in vertebrates rely on several mechanisms including solid barriers against the environment, rapid coagulation of hemolymph after wounding, the formation of aggregates that immobilize and kill foreign invaders, phagocytosis, and the production of antimicrobial peptides. The mode of action and the regulation of the expression of antimicrobial peptides have been studied intensively for more than three decades and are now increasingly well understood. In addition, the characterization of several key molecules involved in other branches of insect immunity has led to a deeper and much more comprehensive understanding of innate immunity in insects. Here we focus on the current status of our view of immunity in the vinegar fly Drosophila melanogaster, the best characterized insect model. We also discuss how evolutionary and ecological forces may have shaped immune responses in Drosophila as compared to other insect species. Finally, several infection models reveal finely-tuned and pathogen-dependent interactions between Drosophila immunity and fly physiology.

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Early membrane exposure of phosphatidylserine followed by late necrosis in murine macrophages induced by Candida albicans from an HIV-infected individual

Cited by 13 publications

References 26 publications

Increased tumour necrosis factor-α production, higher mannose receptor activity and ability to killCandidaby concanavalin-A-activated macrophages

Increased tumour necrosis factor-α production, higher mannose receptor activity and ability to killCandidaby concanavalin-A-activated macrophages

Apoptosis of phagocytic cells induced byCandida albicansand production of IL-10

Mechanisms of Drosophila Immunity - An Innate Immune System at Work

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